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CERTIFICATE
This is to certify that the dissertation titled “A STUDY TO DIFFERENTIATE UPPER AND LOWER URINARY TRACT INFECTIONS WITH BLOOD CRP LEVELS” is the bonafide Original work done by Dr. R.KRISHNA, post graduate student, Institute of Internal medicine, Madras medical college, Chennai-3, in partial Fulfillment of the University Rules and Regulations for the award of MD Branch -1 General Medicine, under our guidance and supervision, during the academic year 2016 - 2019.
Dr.G.SUNDARAMURTHY M.D., Prof. Dr.S.TITO M.D.,
Professor of Medicine, Director(i/c) & Professor, Institute of Internal Medicine Institute of Internal Medicine
Madras Medical College Madras Medical College RGGGH, Chennai – 600 003, RGGGH ,Chennai – 600 003
Prof. Dr. R.JAYANTHI, M.D.,FRCP(GLAS) DEAN,
Madras Medical College & RGGGH Chennai 600 003.
DECLARATION
I, Dr.R . K R I S H N A , solemnly declare that dissertation titled
“A STUDY TO DIFFERENTIATE UPPER AND LOWER URINARY TRACT INFECTIONS WITH BLOOD CRP LEVELS” is a bonafide work done by me at Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai-3 during 2017-18 under the guidance and supervision of Prof. Dr. G.SUNDARAMURTHY, M.D., Professor of Medicine, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai.
This dissertation is submitted to Tamilnadu Dr. M.G.R Medical University, towards partial fulfillment of requirement for the award of M.D.DEGREE IN GENERAL MEDICINE BRANCH-I.
Place: Chennai -03 Dr. R.KRISHNA Date: MD General Medicine, Post Graduate,
Institute of Internal Medicine, Madras Medical College, Chennai – 03
ACKNOWLEDGEMENT
I would like to thank our beloved Dean, Madras Medical College, Prof. Dr. R.JAYANTHI, M.D.,FRCP(GLAS) for her kind permission to use the hospital resources for this study.
I would like to express my sincere gratitude to my beloved Professor and Director(i/c), Institute of Internal Medicine Prof. Dr. S.TITO M.D., for his guidance and encouragement.
With extreme gratitude, I express my indebtedness to my beloved Chief and teacher Prof. Dr. G.SUNDARAMURTHY, M.D., for his motivation, advice and valuable criticism, which enabled me to complete this work.
I am extremely thankful to Assistant Professors of Medicine Dr. KARTHIGEYAN T.S, M.D., and Dr. B.RAMESH, M.D., for their
co-operation and guidance.
I thank the Institute of Biochemistry, Institute of Radiology and Institute of Microbiology for their extreme cooperation extended to me without whom the study would not have been possible.
I thank all Professors, Assistant Professors, and Post-graduates of Institute of Biochemistry, Microbiology and Radiology for their valuable support in the analysis.
I would always remember with extreme sense of thankfulness for the co-operation and criticism shown by my Postgraduate colleagues. I am immensely grateful to the generosity shown by the patients who participated in this study.
Above all, I express my heartfelt gratitude to my parents for their unwavering love, prayers and encouragement. I thank them for being my greatest support, for believing in me and for all the sacrifices they made for me. I would not have reached this far without them.
ABBREVIATION
APN : Acute Pyelonephritis CBC : Complete Blood Count CRP : C-Reactive Protein CT : Computed Tomography
DAMP : Damage Associated Molecular Patterns DM : Diabetes Mellitus
ESBL : Extended spectrum β lactamase
IDSA : Infectious Diseases Society of America LTCF : Long Term Care Facilities
MRSA : Methicillin Resistant Staphylococcus Aureus PAMP :Pathogen Associated Molecular Patterns SGLT : Sodium-glucose Transporter
SMX : Sulfamethoxazole TB : Tuberculosis TMP : Trimethoprim USG : Ultrasonogram
UTI : Urinary Tract Infection VUR : Vesico-Ureteric Reflux WBC : White Blood Cells
XGP : Xanthogranulomatous Pyelonephritis
S.NO TITLE PAGE.NO
1. INTRODUCTION 1
2. AIMS & OBJECTIVES 3
3. REVIEW OF LITERATURE 4
4. MATERIALS AND METHODS 59
5. OBSERVATION AND RESULTS 62
6. DISCUSSION 83
7. CONCLUSION 86
8. LIMITATIONS 87
9. REFERENCES 10. ANNEXURE:
PROFORMA INFORMATION SHEET CONSENT FORM
INSTITUTIONAL ETHICAL COMMITTEE APPROVAL PLAGIARISM REPORT
PLAGIARISM CERTIFICATE MASTER CHART
CONTENTS
1
INTRODUCTION
Urinary tract infection may involve only the lower urinary tract or both the upper and lower tracts. The term cystitis has been used to describe the syndrome involving dysuria, frequency, urgency, and occasionally suprapubic tenderness. However, these symptoms may be related to lower tract inflammation without bacterial infection and can be caused by urethritis (e.g., gonorrhea or chlamydial urethritis).
Furthermore, the presence of symptoms of lower tract infection without upper tract symptoms by no means excludes upper tract infection, which is also often present. Acute pyelonephritis describes the clinical syndrome characterized by flank pain, tenderness, or both, and fever, often associated with dysuria, urgency, and frequency. However, these symptoms can occur in the absence of infection (e.g., in renal infarction or renal calculus).A more rigorous definition of acute pyelonephritis is the previously described syndrome accompanied by significant bacteriuria and acute infection in the kidney. Uncomplicated urinary tract infection refers to infection in a structurally and neurologically normal urinary tract. Complicated urinary tract infection refers to infection in a urinary tract with functional or structural abnormalities, including indwelling catheters and calculi[1]. In general, infection in men, pregnant women, children, and patients who are hospitalized or in health care–
2
associated settings may be considered complicated. In the patient with complicated infection, infecting microorganisms are more likely to be resistant to antimicrobial agents.
3
AIMS AND OBJECTIVES
To explore a diagnostic method to differentiate for upper and lower urinary tract Infections.
4
REVIEW OF LITERATURE
Urinary tract infection
In adults UTI can be classified into 5 groups[2]
• Uncomplicated cystitis in women
• Recurrent cystitis in women
• Acute uncomplicated pyelonephritis in women
• Complicated UTI
• Asymptomatic bacteriuria
Complicated UTI
It is defined as urinary tract infection that increases risk for serious complications or treatment failure.
Complicated UTIs may require different pre treatment and post treatment evaluation and duration of anti-microbial treatment than for UN complicated UTI. Occasionally complicated UTIs are diagnosed after a poor response to treatment.
5
Factors modulating risk of acute uncomplicated urinary tract infections in women:
picture 1:Factors complicating Uncomplicated UTI in women
6 Epidemiology
The incidence of acute cystitis in sexually active women is about 0.5 per 1 person year[3]. The incidence of acute pyelonephritis in young women is about 3/1000 person –years[4]. The incidence of symptomatic urinary tract infection in adult men less than 50 years is much lower than seen in women ranging from 5 to 8 /10000 men annually.
Nosocomial urinary tract infections are a common cause of complicated UTI which occurs in 5% of admission in tertiary care hospitals. In hospitalized patients , catheter associated bacteriuria is the most common source of gram-negative bacteremia[5].
Asymptomatic bacteriuria is defined as presence of 105 or more colony forming units per ml of the organism in 2 separate consecutive clean voided urine specimen in the absence of symptom related to the urinary tract[6]. It is found in about 5% of adult young women[7] and very rarely in men less than 50 years.
7 Pathogenesis
Uncomplicated infection
Most of uncomplicated UTIs in healthy women result when organisms such as E.coli present in rectum enter the urinary bladder after an interim phase of distal urethral colonization. Staphylococcus aureus seed the urinary tract by hematogeneous spread.
The protective factors from urinary tract infection include
− Host‘s immune response
− Maintanence of normal vaginal flora
− Removal of urinary bladder bacteriuria by micturition[8] .
P-fimbriated Strains of Escherichia coli are associated with acute uncomplicated pyelonephritis. Their adherence properties stimulate epithelial and other cells to produce inflammatory factors that stimulate the inflammatory response[9] .
8 Figure 2.
9 The determinants of virulence include
o Adherence factor (type 1, S, and Dr fimbriae) o Toxins(hemolysin)
o Immune evasion
o Iron acquisition(aerobactin) o Flagella
o serum resistance [10]
The factors responsible for decreased prevalence of UTI in men include;
i. Greater distance between the anus and the urethral meatus ii. Drier environment surrounding male urethra
iii. Greater length of male urethra
Risk factors for urinary tractinfection in young healthy men include;
¾ Intercourse with an infected female partner
¾ Anal intercourse
¾ Lack of circumcision
10 Complicated infection ;
The predisposing factors that lead to complicated UTI include;
o Obstruction or stasis of urine flow
o Facilatiting entry of organisms into urinary tract by bypassing host defence mechanisms
o Providing a nidus for infection not readily treatable with antimicrobials
o Compromising the host immune system
Complicated UTIs occur in settings of impaired host defence such as
¾ Indwelling catheter use
¾ VUR
¾ Obstruction
¾ Neutropenia
¾ Immune deficiencies
Diabetes mellitus is associated with syndromes of complicated UTI including
1. Renal and perirenal abscess
2. Emphysematous pyelonephritis and cystitis 3. Papillary necrosis
4. Xanthogranulomatous pyelonephritis
11
The virulence of the pathogens are less important in the pathogenesis of complicated urinary tract infections compared with uncomplicated urinary tract infections.But,multidrug resistance is more likely with complicated urinary tract infections.
Figure 3.
12 ETIOLOGICAL AGENTS;
BACTERIAL ETIOLOGY OF URINARY TRACT INFECTIONS
Picture 4:Bacterial organisms causing UTI
13
Uncomplicated upper and lower urinary tract infections are most often caused by Escherichia coli in 70% to 95% and staphylococcus saphrophyticus present in 5% to 20%. The common contaminants in healthy non-pregnant women include lactobacilli, enterococci, coagulase negative staphylococcus and group B streptococci.
E.coli is the most common bacteria in complicated UTIs.
Other organisms include citrobacter spp.,Enterobacter spp., enterococci, pseudomonas aeruginosa,staph.aureus. UTIs caused by fungi ,especially candida spp., is increasing. Polymicrobial and multidrug resistant infections are more likely in patients with chronic conditions such as neurogenic bladder and spinal cord injury.
Figure 5. Factors that promote the recurrence of UTI
14 CLINICAL SYNDROMES
Figure 6.
Acute uncomplicated cystitis in young women;
They present with symptoms such as acute onset of dysuria,frequency,urgency or suprapubic pain. In a sexually active young women acute cystitis usually presents with acute dysuria. Neisseria gonorrhoeae,chlamydia trachomatis,or herpes simplex virus infections presents with acute urethritis. Candida spp. Or Trichomonas vaginalis presents with vaginitis.Definitive diagnosis of urinary tract infection
15
requires the presence of significant bacteriuria ,which is 105 or more uropathogens per ml of midstream voided urine. The IDSA ( Infectious Diseases Society of America) consensus definition of cystitis is 103 cfu per milliliter or more uropathogens[11].Generally,urine cultures are not required in women with uncomplicated cystitis because patient’s history is highly reliable in establishing the diagnosis[12].
Increasing resistance is often encountered for E.coli in uncomplicated UTIs to sulfonamides, amoxicillin, cotrimoxazole.
Nitrofurantoin resistance to E.coli is less than 5%,although it is inactive against proteus spp. And some klebsiella spp and Enterobacter.In uncomplicated cystitis, E.coli strains are susceptible to fluoroquinolones although resistance is increasing in many parts of the world[13,14]. Infections caused by ESBL (extended spectrum β-lactamase) producing strains are increasing in number in addition,even in the setting of uncomplicated urinary tract infection.
Recurrent Acute Uncomplicated Cystitis in Women
Much recurrent cystitis in healthy women is caused by persistence of the initially infecting strain in the fecal flora[15]. Experimental studies in mice also suggest that some same-strain recurrent UTIs may be caused by a latent reservoir of uropathogens in the bladder
16
epithelium that persist after the initial UTI[16], and indirect evidence indicates that this may occur in humans[17]. If the recurrence is within 1 or 2 weeks of treatment, an antimicrobial-resistant uropathogen should be considered, and a urine culture should be performed followed by treatment with an alternative regimen.
Acute Uncomplicated Pyelonephritis in Women
Acute pyelonephritis is suggested by fever (temperature ≥38° C), chills, flank pain, nausea and vomiting, and costovertebral angle tenderness. Cystitis symptoms are variably present. Symptoms may vary from a mild illness to a sepsis syndrome with or without shock and renal failure. Pyuria is almost always present, but leukocyte casts, specific for UTI, are infrequently seen. Gram stain of the urine sediment may aid in differentiating gram-positive and gram-negative infections, which can influence empiric therapy. A urine culture, which should be performed in all women with acute pyelonephritis, will have 104 cfu/ml or more of uropathogens in up to 95% of patients[11]. On pathologic examination, the kidney shows a focal inflammatory reaction with neutrophil and monocyte infiltrates, tubular damage, and interstitial edema . Although imaging studies are generally not performed, the infected kidney is often enlarged, and contrast enhanced computed tomography (CT) shows
17
decreased opacification of the affected parenchyma, typically in patchy, wedge-shaped, or linear patterns.
Picture 6:Histopathology of Acute Pyelonephritis
Complicated Infections
Patients with complicated UTI may present with classic signs of cystitis and pyelonephritis but also may have vague or nonspecific symptoms, such as fatigue, irritability, nausea, headache, and abdominal or back pain. Acute cystitis in healthy individuals other than young women is more likely to involve occult renal or prostatic infection and may respond poorly to short-course therapy. Noninvasive tools to localize
18
infections to the kidney or prostate are lacking, so clinical estimation of risk in a given patient is imprecise. Some patients, such as those who are diabetic or pregnant, warrant special attention because of the serious complications that can occur if treatment is inadequate. Urethritis must be excluded in dysuric sexually active men by a urethral Gram stain or a first-voided urine specimen wet-mount evaluation for urethral leukocytosis.
Complicated UTI, as with uncomplicated infection, is generally associated with pyuria and bacteriuria, although these may be absent if the infection does not communicate with the collecting system.
Urine culture should always be performed in patients with suspected complicated UTI. The IDSA consensus definition of complicated UTI is 105 cfu/ml or more in the urine of women and 104 cfu/ml or more in men, but lower counts in symptomatic persons, as demonstrated in patients with uncomplicated UTI, may well represent significant bacteriuria. This is especially true when the specimen is collected from a urinary catheter. Thus it is reasonable to use a colony count threshold of 103 cfu/ml of uropathogens to diagnose complicated UTI.
19 Catheter-Associated Infections;
Approximately 15% to 25% of patients in general hospitals have a urethral catheter inserted at some time during their stay, and approximately 5% to 10% of long-term care facility residents are managed with urethral catheterization, in some cases for years. The incidence of bacteriuria associated with indwelling catheters is 3% to 10% per day of catheterization, and the duration of catheterization is the most important risk factor for the development of catheter-associated bacteriuria.
Catheter-associated bacteriuria is the most common source of gram negative bacteremia in hospitalized patients. Complications of long-term catheterization (≥30 days) include almost universal bacteriuria, often with multiple antibiotic-resistant flora, and (in addition to cystitis, pyelonephritis, and bacteremia, as seen with short-term catheterization) frequent febrile episodes, catheter obstruction, stone formation associated with urease-producing uropathogens, and local genitourinary infections.
Other rare complications include fistula formation and bladder cancer. An increase in mortality risk has been reported with catheter associated bacteriuria, but it is difficult to distinguish the role of the catheter because most deaths occur in patients who have severe underlying disease.
20 Spinal Cord Injury;
Spinal cord injury alters the dynamics of voiding and often
requires the use of bladder drainage with catheters. The diagnosis of UTI in patients with spinal cord injuries is often problematic and is based on the combination of symptoms and signs (which are often nonspecific), pyuria, and significant bacteriuria.
Prostatitis;
Prostatitis occurs in up to 25% of men during their lifetime, but it is caused by acute or chronic bacterial infection in a minority[18].
The most common organisms causing bacterial prostatitis are
gram-negative bacilli, including E. coli, Proteus spp., Klebsiella spp., P.aeruginosa, and, less frequently, enterococci and S. aureus. The pathogenesis of prostatitis is believed to be related to reflux of infected urine from the urethra into the prostatic ducts. Prostatic calculi, commonly found in adult men, may provide a nidus for bacteria and protection from antibacterial agents.Acute bacterial prostatitis is rare.
Patients present with dysuria, frequency,urgency, obstructive voiding symptoms, fever, chills, and myalgias.The prostate is tender and swollen.
Prostatic massage, as a diagnostic test, is contraindicated in men in whom the diagnosis of acute prostatitis is being considered because of the risk
21
for precipitating bacteremia. The patient will usually have pyuria and a positive urine culture.re usually present in quantities of 105 cfu/ml or more.
Chronic bacterial prostatitis is characterized by recurrent UTIs with the same uropathogen with intervening asymptomatic periods.
The prostate typically is normal to palpation during asymptomatic periods.Chronic bacterial prostatitis is characterized microscopically by the presence of 10 or more leukocytes per high-power field in expressed prostatic secretions or postmassage voided urine in the absence of significant pyuria in first-voided and midstream urine specimens, as well as a uropathogen colony count at least 10-fold higher in the expressed prostatic secretions or postmassage voided urine compared with the first- voided midstream urine. In addition, macrophage-laden fat droplets (oval fat bodies) are usually prominent in the prostatic secretions.
Renal Abscess;
Renal cortical and cortico medullary abscesses and perirenal abscesses occur in 1 to 10 per 10,000 hospital admissions[19] .Patients usually present with fever, chills, back or abdominal pain, and costovertebral angle tenderness, but they may have no urinary symptoms or findings if the abscess does not communicate with the collecting system, as often occurs with a cortical abscess. Bacteremia may be
22
primary (cortical abscess) or secondary (corticomedullary or perirenal).
The clinical presentation may be insidious and nonspecific, especially with perirenal abscess, and the diagnosis may not be made until admission to a hospital or at autopsy. CT is recommended to establish the diagnosis and location of a renal or perirenal abscess. A renal cortical abscess (renal carbuncle) is usually caused by S.aureus, which reaches the kidney by hematogenous spread. A renal corticomedullary abscess, in contrast, usually results from ascending UTI in association with an underlying urinary tract abnormality, such as obstructive uropathy or VUR, and is usually caused by common uropathogenic species such as E.
coli and other gram-negative bacilli. Such abscesses may extend deep into the renal parenchyma, perforate the renal capsule, and form a perirenal abscess. Perirenal abscesses usually occur in the setting of obstruction or other complicating factors and result from ruptured intrarenal abscesses, hematogenous spread, or spread from a contiguous infection. Causative uropathogens are those usually found in complicated UTIs, including S. aureus and enterococci; polymicrobial infections are common. Anaerobes or Mycobacterium tuberculosis may be causative.
23 Papillary Necrosis
More than half of patients who develop papillary necrosis have
diabetes, almost always in conjunction with a UTI, but the condition also complicates sickle cell disease, analgesic abuse, and obstruction. Renal papillae are vulnerable to ischemia because of the sluggish blood flow in the vasa recta, and relatively modest ischemic insults may cause papillary necrosis. The clinical features are those typical of pyelonephritis. In addition, passage of sloughed papillae into the ureter may cause renal colic, renal impairment or failure, or obstruction with severe urosepsis.
Papillary necrosis in the setting of pyelonephritis is associated with pyuria and a positive urine culture. Causative uropathogens are those typical of complicated UTI. CT is the preferred diagnostic procedure.
Radiologic findings include an irregular papillary tip; dilated calyceal fornix; extension of contrast material into the parenchyma; and a separated crescent-shaped papilla surrounded by contrast, called the ring sign
24 Figure 7.
Emphysematous Pyelonephritis
Emphysematous pyelonephritis is a fulminant, necrotizing, life- threatening variant of acute pyelonephritis caused by gas-forming organisms, including E. coli, Klebsiella pneumoniae, P. aeruginosa, and Proteus mirabilis[20]. Up to 90% of cases occur indiabetic patients, and obstruction may be present. Symptoms are suggestive of pyelonephritis, and there may be a flank mass. Dehydration and ketoacidosis are common. Pyuria and a positive urine culture are usually present. Gas is usually detected by a plain abdominal radiograph or ultrasound . CT is
25
the diagnostic modality of choice, however, because it can localize the gas better than ultrasound. Accurate localization of gas is important because gas also may form in an infected obstructed collecting system or renal abscess; although serious, these conditions do not carry the same poor prognosis and are managed differently.
Renal Malacoplakia
Malacoplakia is a chronic granulomatous disorder of unknown
etiology involving the genitourinary, gastrointestinal, skin, and pulmonary systems[21]. It is characterized by an unusual inflammatory reaction to a variety of infections and is manifested by the accumulation of macrophages containing calcified bacterial debris called Michaelis- Gutmann bodies . The underlying disorder appears to be a monocyte- macrophage bactericidal defect. The diagnosis is made by histologic examination of involved tissue. Genitourinary malacoplakia, most often involving the bladder, is usually associated with gram-negative UTI.
Patients with renal malacoplakia generally have fever, flank pain, pyuria and hematuria, bacteriuria, and, if both kidneys are involved, impaired renal function. CT usually shows enlarged kidneys with areas of poor enhancement, and the condition may be indistinguishable from other infectious or neoplastic lesions. On occasion, the malacoplakia may
26
extend through the renal capsule into the perinephric space, simulating a renal carcinoma.
Picture 8:Renal Malacoplakia
Xanthogranulomatous Pyelonephritis
Xanthogranulomatous pyelonephritis is a poorly understood,
uncommon but severe chronic destructive granulomatous inflammation of renal parenchyma associated with obstruction and infection of the urinary tract[22]. The renal parenchyma is replaced with a diffuse or segmental cellular infiltrate of foam cells, which are lipid-laden macrophages. The process also may extend beyond the renal capsule to the retroperitoneum.
Its pathogenesis appears to be multifactorial, with infection complicating obstruction and leading to ischemia, tissue destruction, and accumulation of lipid deposits. Patients with xanthogranulomatous pyelonephritis are characteristically middle-aged women and have chronic symptoms such
27
as flank pain, fever, chills, and malaise. Flank tenderness, a palpable mass, and irritative voiding symptoms are common. The urine culture is usually positive with E. coli, other gram-negative bacilli, or S. aureus. CT generally shows an enlarged nonfunctioning kidney, often the presence of calculi and low-density masses (xanthomatous tissue), and in some cases, involvement of adjacent structures . It may be difficult to distinguish from neoplastic disease.
Asymptomatic Bacteriuria
Asymptomatic bacteriuria is common and generally benign. Pyuria is often present, especially in elderly people, and is a predictor for subsequent symptomatic UTI in some groups. Causative uropathogens are the same as those causing UTIs in the same population. Screening for and treatment of asymptomatic bacteriuria is generally not warranted. In young women with recurrent UTI, asymptomatic bacteriuria may be protective against symptomatic recurrence and treatment may increase the risk for such recurrences[23]. However, patients at high risk for serious complications warrant a more aggressive approach to diagnosis and treatment, including pregnant women and patients undergoing urologic surgery. Current management strategies in patients with a renal transplant, including long-term antimicrobial prophylaxis, help prevent both asymptomatic bacteriuria and symptomatic UTI. It is not clear,
28
however, whether screening for or treatment of asymptomatic bacteriuria in such patients is worthwhile. Some authorities advise treatment of asymptomatic bacteriuria found in patients with anatomic or functional abnormalities of the urinary tract, diabetic patients, and patients with urea-splitting bacteria (e.g., P. mirabilis, Klebsiella spp.). Evidence based guidelines for screening and treatment of asymptomatic bacteriuria in these populations are needed.Asymptomatic bacteriuria in catheterized patients in hospitals and longterm care facilities, although thought to be generally benign, represents a large reservoir of antimicrobial-resistant urinary pathogens that increases the risk for cross-infection among catheterized patients and results in frequent inappropriate antimicrobial use[24].
INVESTIGATIONS;
Urinalysis
specimen collection
Specimens must be collected in clean, dry, leak-proof containers.
Disposable containers should be used because they eliminate the chance of contamination owing to improper washing. These disposable containers are available in a variety of sizes and shapes, including bags with adhesive for the collection of pediatric specimens and large
29
containers for 24-hour specimens. Properly applied screw-top lids are less likely to leak than are snap-on lids. Containers for routine urinalysis should have a wide mouth to facilitate collections from female patients and a wide,flat bottom to prevent overturning. They should be made of a clear material to allow for determination of color and clarity. The recommended capacity of the container is 50 mL, which allows 12 mL of specimen needed for microscopic analysis, additional specimen for repeat analysis, and enough room for the specimen to be mixed by swirling the container. Individually packaged sterile containers with secure closures should be used for microbiologic urine studies. Sterile containers are also suggested if more than 2 hours elapse between specimen collection and analysis. Specially designed sterile containers are available that have a lid with a transfer device that can be assessed with a device called a transfer straw. The transfer straw has a needle and an evacuated tube holder.
Urine can be sterilely transferred to tubes containing preservatives for microbiology testing and tubes with conical bottoms for sediment analysis or round bottoms for automated reagent strip testing.
Specimen Preservation
The most routinely used method of preservation is refrigeration at 2°C to 8°C, which decreases bacterial growth and metabolism. If the urine is to be cultured, it should be refrigerated during transit and kept
30
refrigerated until cultured up to 24 hours. The specimen must return to room temperature before chemical testing by reagent strips. When a specimen must be transported over a long distance and refrigeration is impossible, chemical preservatives may be added. Commercially prepared transport tubes are available. The ideal preservative should be bactericidal, inhibit urease, and preserve formed elements in the sediment. The most routinely used method of preservation is refrigeration at 2°C to 8°C, which decreases bacterial growth and metabolism. If the urine is to be cultured, it should be refrigerated during transit and kept refrigerated until cultured up to 24 hours. The specimen must return to room temperature before chemical testing by reagent strips. When a specimen must be transported over a long distance and refrigeration is impossible, chemical preservatives may be added. Commercially prepared transport tubes are available. The ideal preservative should be bactericidal, inhibit urease, and preserve formed elements in the sediment.
Midstream Clean-Catch Specimen
As an alternative to the catheterized specimen, the midstream clean-catch specimen provides a safer, less traumatic method for obtaining urine for bacterial culture and routine urinalysis. It provides a specimen that is less contaminated by epithelial cells and bacteria and,
31
therefore, is more representative of the actual urine than the routinely voided specimen. Patients must be provided with appropriate cleansing materials, a sterile container, and instructions for cleansing and voiding.
Strong bacterial agents, such as hexachlorophene or povidone-iodine, should not be used as cleansing agents. Mild antiseptic towelettes are recommended. Some urine collection transfer kits contain Castile Soap Towelettes.
Suprapubic Aspiration
Occasionally urine may be collected by external introduction of a needle through the abdomen into the bladder. Because the bladder is sterile under normal conditions, suprapubic aspiration provides a sample for bacterial culture that is completely free of extraneous contamination.
The specimen can also be used for cytologic examination.
Bacteria
Bacteria are not normally present in urine. However, unless specimens are collected under sterile conditions (catheterization), a few bacteria are usually present as a result of vaginal, urethral, external genitalia, or collection-container contamination. These contaminant bacteria multiply rapidly in specimens that remain at room temperature for extended periods, but are of no clinical significance. They may
32
produce a positive nitrite test result and also frequently result in a pH above 8, indicating an unacceptable specimen. Bacteria may be present in the form of cocci (spherical) or bacilli (rods). Owing to their small size, they must be observed and reported using high-power magnification.
They are reported as few, moderate, or many per high-power field.To be considered significant for UTI, bacteria should be accompanied by WBCs. Some laboratories report bacteria only when observed in fresh specimens in conjunction with WBCs . The presence of motile organisms in a drop of fresh urine collected under sterile conditions correlates well with a positive urine culture. Observing bacteria for motility also is useful in differentiating them from similarly appearing amorphous phosphates and urates. The use of phase microscopy aids in the visualization of bacteria.
Microscopic Examination
Much can be learned from simple microscopic examination of urine. A drop of fresh uncentrifuged urine placed on a slide, covered with a coverglass, and examined with restricted light intensity under the high- dry objective of an ordinary clinical microscope can reveal leukocytes, epithelial cells, and bacteria if more than 105/mL are present. Finding 105 organisms per milliliter in a properly collected and examined urine specimen is strong evidence of active urinary tract infection. A Gram
33
stained smear of uncentrifuged midstream urine that shows gram-negative rods is diagnostic of a urinary tract infection.
Brief centrifugation of urine readily sediments pus cells, which may carry along bacteria and thus may help in microscopic diagnosis of infection. The presence of other formed elements in the sediments—or the presence of proteinuria—is of little direct aid in the specific identification of active urinary tract infection. Pus cells may be present without bacteria, and, conversely, bacteriuria may be present without pyuria. The presence of many squamous epithelial cells, lactobacilli, or mixed flora on culture suggests improper urine collection. Some urine dipsticks contain leukocyte esterase and nitrite, measurements of polymorphonuclear cells and bacteria, respectively, in the urine. Positive reactions are strongly suggestive of bacterial urinary tract infection.
Although not readily embraced by clinical microbiology laboratories, many chemistry laboratories have implemented automated or semiautomated instruments for routine performance of urinalysis. A variety of techniques are used by these instruments to detect leukocytes and bacteria. The performance of these systems varies, but they bring a level of standardization for high-volume testing that may not be accomplished using dipstick methods.
34 Culture
Culture of the urine, to be meaningful, must be performed quantitatively. Properly collected urine is cultured in measured amounts on solid media, and the colonies that appear after incubation are counted to indicate the number of bacteria per milliliter. The usual procedure is to spread 0.001–0.05 mL of undiluted urine on blood agar plates and other solid media for quantitative culture. All media are incubated overnight at 37°C; growth density is then compared with photographs of different densities of growth for similar bacteria, yielding semiquantitative data. In active pyelonephritis, the number of bacteria in urine collected by ureteral catheter is relatively low. While accumulating in the bladder, bacteria multiply rapidly and soon reach numbers in excess of 105/mL—far more than could occur as a result of contamination by urethral or skin microbiota or from the air. Therefore, it is generally agreed that if more than 105 colonies/mL are cultivated from a properly collected and properly cultured urine specimen, this constitutes strong evidence of active urinary tract infection. The presence 105 bacteria or more of the same type per milliliter in two consecutive specimens establishes a diagnosis of active infection.
35 ULTRASOUND
The infection may be either acute or chronic. Ultrasound signs of renal infection may be absent altogether, and this is the commonest scenario as the infective episode has often been successfully treated with antibiotics by the time the ultrasound scan is performed. The infection may be confined to the bladder, that is cystitis, in which case low-level echoes and/or hyperechoic debris may be identified, or may have progressed to the kidneys. Scarring and/or cortical thinning may be present in cases of repeated infections.
Pyelonephritis
Acute pyelonephritis
Acute inflammation of the kidney rarely results in any ultrasound abnormality. Occasionally the kidney may be enlarged and hypoechoic, the contrast between the kidney and the hepatic or splenic parenchyma increasing due to oedema, but the ultrasound changes are generally subtle. The normally clear differentiation between the cortex and the medullary pyramids may become indistinct, but again may go unrecognized. CT is useful for detecting subtle inflammatory changes within the kidney.
36
Figure 9.
Chronic pyelonephritis
This chronic inflammatory state is usually the result of frequent previous inflammatory/infective episodes. The kidney may be small and often has focal scarring present. Scar tissue has the appearance of a hyperechoic, linear lesion which affects the smooth renal outline and crosses the renal cortex . (Do not confuse focal scarring with fetal lobulation: the latter is smooth, thin, continuous with the capsule and forms an indentation between the pyramids.) The renal cortex is frequently thin in chronic pyelonephritis and may appear abnormally hyperechoic.
37
Figure 10.
Bladder diverticula
Repeated infections can cause the bladder wall to thicken and become trabeculated. In such cases, a bladder diverticulum may form, making treatment of subsequent infections particularly difficult. The diverticulum may harbour debris or stones and may fail to empty properly, often enlarging as the urine refluxes into it when the patient micturates .
Focal pyelonephritis
The presence of acute infection within the kidney may progress in focal regions of the renal parenchyma. This phenomenon is particularly associated with diabetics. The ultrasonic changes are subtle, as in diffuse pyelonephritis, but it is possible to detect a slight change in echogenicity when it is surrounded by normal-looking parenchyma. Focal
38
pyelonephritis (sometimes called focal nephronia) may be either hypo- or hyperechoic compared with normal renal tissue. Depending on the size of the lesion, it may cause a mass effect, mimicking a renal tumour. The outline of the kidney is preserved, however the patient presents with fever and tenderness on the affected side and frequently has a history of urinary tract infection. A focal renal mass under these circumstances is highly suggestive of focal pyelonephritis and is also well demonstrated on CT[25]. It usually responds to antibiotic therapy and resolution of the lesion can be monitored with ultrasound scans. Focal pyelonephritis can progress to form an abscess in the kidney, which can normally be treated by percutaneous drainage and antibiotics.
Renal abscess
A renal abscess is generally a progression of focal inflammation within the kidney. The area liquefies and may enlarge to form a complex mass with distal acoustic enhancement. Low-level echoes from pus may fill the abscess cavity, giving it the appearance of increased echogenicity, but it may also be hypoechoic. The margins of the abscess may be ill- defined at first but may develop a more obvious capsule as the lesion becomes established , this capsule often has an easily identifiable thick rim. Flow may be seen in the inflammatory capsule with colour Doppler, but not in the liquefied centre. A renal abscess may mimic a lymphoma as
39
both may be hypoechoic on ultrasound, and both may have either single or multiple foci. The abscess may be intrarenal, subcapsular or perirenal.
Frequently, drainage under ultrasound guidance is the preferred treatment; gradual resolution of the abscess can also be monitored with ultrasound.
Picture 11:CT image of Renal abscess
Tuberculosis (TB)
Renal TB is an uncommon finding and a difficult diagnosis to make on ultrasound. The subtle inflammatory changes which affect the calyces in the early stages are best demonstrated with CT. In the later
40
stages ultrasound may show calcific foci and obstructed calyces as a result of thickened inflammatory calyceal walls, calcification and debris.
TB frequently spreads to other adjacent sites in the abdomen, including the psoas muscle and gastrointestinal tract. The differential diagnosis is xanthogranulomatous pyelonephritis, which is often indistinguishable from TB on ultrasound, or a necrotic renal neoplasm.
Figure 12.
41
Xanthogranulomatous pyelonephritis (XGP)
This condition (which gets its name from the yellow colour of the kidney) is the result of renal obstruction by calculi in the pelvicalyceal system. Frequently, a staghorn calculus is responsible. The kidney becomes chronically infected and the calyces enlarge and become filled with infected debris. The cortex may be eroded and thin. On ultrasound, these appearances are similar to TB or to a pyonephrosis. The latter is usually accompanied by a more severe, acute pain and fever whereas XGP or TB has a lower-grade, chronic pain. CT may differentiate TB from XGP and is also more sensitive to extrarenal spread of disease.
CT SCAN
Acute pyelonephritis
CT is the modality of choice for evaluating the parenchymal involvement of acute pyelonephritis, sometimes referred to as acute bacterial nephritis. It provides comprehensive anatomic and physiologic information that accurately characterizes both intrarenal and extrarenal pathologic conditions. Unenhanced CT is excellent for identifying urinary tract gas, calculi, hemorrhage, renal enlargement, inflammatory masses, and obstruction[26]. However, unenhanced CTimages may appear normal.
On postcontrast studies, acute bacterial nephritis most commonly
42
manifests as one or more wedge-shaped areas or streaky zones of lesser enhancement that extend from the papilla to the renal cortex in the nephrographic phase, also known as striated nephrogram. In the delayed phase, reversal of the striated nephrogram occurs. Other findings include enlargement of the affected kidney due to edema, perinephric stranding, and areas of increased attenuation if hemorrhagic bacterial nephritis is present and thickening of the renal pelvis and ureteric wall. In progressive cases, a parenchymal abscess may develop. On CT, before liquefaction becomes evident, the abscess may resemble a renal mass, especially in the absence of typical clinical findings. Abscesses typically appear as round or geographic low-attenuation collections that do not enhance centrally but may have an enhancing rim . The rims are pseudocapsules with varied wall thicknesses and frequent nodularity. A halo of diminished enhancement may surround the abscess during the nephrographic phase. Extraparenchymal collections occasionally extend into adjacent structures, such as the psoas muscle. Persistent urinary leukocytes indicate residual inflammation that can usually be detected on CT[27,28].
43
Picture 13:CT image of Acute Pyelonephritis
Chronic pyelonephritis
Imaging findings include renal scarring, atrophy, and cortical thinning; hypertrophy of residual normal tissue (which may mimic a mass lesion); calyceal clubbing secondary to retraction of the papilla from the overlying scar; dilatation of the calyceal system; and overall renal asymmetry.
Emphysematous Pyelonephritis
Two types of gas distribution have been reported. Type 1 (33 % of cases) is more aggressive and is characterized by renal parenchymal destruction that manifests with streaky or mottled areas of gas without intrarenal or extrarenal fluid collections . Type 2 (66 %) is less aggressive
44
andis characterized by renal or perirenal fluid collections associated with bubbly or loculated gas or by gas in the urinary collecting system.
Xanthogranulomatous Pyelonephritis
Diffuse (>80 %) or segmental imaging findings may be present. In the segmental form, the process may have the appearance of a renal mass and may be indistinguishable from RCC. In the more common diffuse form, the kidney is enlarged, with poor or no function. When extension occurs outside the kidney, it may involve the psoas muscle, and there may be fistulas to the abdominal wall. Most cases occur in association with a renal pelvic calculus; thus, hydronephrosis is thought to be a contributing factor[29]. CT is the imaging modality of choice for diagnosis and management. Findings include an enlarged kidney, with decreased or absent function; peripheral cystic dilatation; enhancing walls of the abscess cavities; perinephric extension; and a large central calculus.
Stones are often laminated or branching in appearance.
45 C Reactive Protein
CRP and many other APR can influence multiple stages of inflammation, and CRP has both pro inflammatory and anti inflammatory actions, although the primary effect may be anti inflammatory[30,31] . CRP can promote the recognition and elimination of pathogens and enhance the clearance of necrotic and apoptotic cells[32-38]. The protein consists of five identical, non-covalently associated subunits, each with a molecular weight of approximately 23 kD, which are arranged symmetrically around a central pore[39] . CRP and related proteins with this structure are termed pentraxins, which are a family of pattern recognition molecules involved in the innate immune response; others include serum amyloid P and a number of pattern recognition molecules referred to as long
Picture 15:CT image of XGPN
46
pentraxins. A major function of CRP is its ability to bind phosphocholine, thereby permitting recognition both of foreign pathogens that display this moiety and phospholipid constituents of damaged cells . CRP can also activate the complement system and bind to phagocytic cells via Fc receptors, suggesting that it can initiate elimination of pathogens and targeted cells by interaction with both humoral and cellular effector systems of inflammation. These functions of CRP may have negative effects in some settings. As an example, CRP levels are increased in patients with immune thrombocytopenia (ITP), where CRP may amplify antibody-mediated platelet destruction upon binding to phosphocholine that is exposed after oxidation triggered by anti platelet antibodies. Pro inflammatory effects of CRP include activation of the complement system and the induction in monocytes of inflammatory cytokines and tissue factor and shedding of the IL-6 receptor . As a result, the CRP response to tissue injury may worsen tissue damage in some settings .
C-reactive protein — Elevations of CRP occur in association with acute and chronic inflammation due to a range of causes, including infectious diseases and non infectious inflammatory disorders. Very small changes in CRP levels, detected with highly-sensitive assays, may also occur in association with metabolic stresses in the absence of acute or chronic inflammatory states as they have traditionally been viewed.
47 'Normal' CRP levels
The level of CRP that is truly normal or clinically innocuous is not known. Data from a study conducted by the National Health and Nutrition Evaluation Survey of over 21,000 people in the United States revealed that CRP levels vary with age, sex, and race, with slightly higher levels seen with increased age, with female sex, and in African Americans . A rough correction of the CRP for age can be made by using the following formulas: the upper limit of the reference range (mg/dL) equals (age in years)/50 for men and (age in years/50) + 0.6 for women[40,41] . It is very important to note that there is no uniformity in the units that are used to report CRP levels. Some laboratories report CRP concentrations as mg/dL while others employ mg/L. Standard CRP determinations may be reported either in units of mg/dL or in units of mg/L, while determinations using a highly sensitive assay, generally referred to as "high-sensitivity CRP" (hs-CRP), are routinely reported in units of mg/L. Population studies reveal a skewed, rather than Gaussian, distribution of plasma CRP concentrations. About 70 to 90 percent of samples from reference populations have CRP concentrations under 0.3 mg/dL (3 mg/L), but some individuals have minor elevations up to 1 mg/dL (10 mg/L). What we commonly call normal ranges (properly called reference ranges) for CRP vary greatly from one laboratory to
48
another, to a degree that cannot be explained on a biologic or technical basis. What is thus regarded as "elevated" is often misleading. It would be best to regard CRP concentrations >1 mg/dL (10 mg/L) as indicating clinically significant inflammation while concentrations between 0.3 and 1 mg/dL (3 and 10 mg/L) indicate what is commonly referred to as low- grade inflammation. Low-grade inflammation is not accompanied by the classic signs of inflammation and may result from an immense number of metabolic stresses . Some of these stresses are clinically apparent;
examples include atherosclerosis, obesity, obstructive sleep apnoea, insulin resistance, hypertension, and type 2 diabetes. Low grade inflammation is, however, also associated with an astounding number of conditions and lifestyles known to be associated with poor health, including low levels of physical activity, prehypertension , a large variety of unhealthy diets, social isolation, and even being unmarried .
Moderate to marked elevation of CRP — In most inflammatory conditions, the CRP, like the ESR, becomes elevated as part of the acute phase response. Markedly elevated levels of CRP are strongly associated with infection. Infections, most often bacterial, were found in approximately 80 percent of patients with values in excess of 10 mg/dL (100 mg/L) and in 88 to 94 percent of patients with values over 50 mg/dL (500 mg/L). Levels of CRP may also be elevated in patients with viral
49
infections, although usually not to the degree seen in patients with bacterial infection .ESR and CRP levels may be discrepant due to differences in kinetics, with the CRP both rising and decreasing more rapidly; or related to characteristics of the inflammatory or and immune- disease related mechanisms, as in systemic lupus, where significant CRP elevations are typically not as common or to as great a degree as are increases in the ESR.
High-sensitivity CRP and low-grade inflammation;
Some confusion has arisen because of widespread use of the terms
"high-sensitivity CRP" and "low-grade inflammation" . One common misunderstanding has been the incorrect belief that hs-CRP is different in some way from the CRP that has been measured for many years. It is not.
"High-sensitivity" only means that the concentration of CRP was determined using an assay designed to measure and distinguish very low levels of CRP. The CRP that is measured has no new or unique properties . Minor CRP elevation (concentrations between 3 and 10 mg/L) has been generally regarded as a marker of what has been called low-grade inflammation. However, this poorly defined state, sometimes referred to as mini inflammation or subclinical inflammation, occurs in many conditions in which there are minor degrees of metabolic dysfunction, such as obesity and insulin resistance, unlike inflammation as it has
50
traditionally been understood. Moreover, the low-grade inflammatory state differs in several important ways from the acute inflammation that occurs in response to infection or tissue injury[42,43]. The acute inflammatory state is associated with the classic signs of inflammation (swelling, erythema, warmth, and pain), while low-grade inflammation is not. Acute inflammation generally shows a marked CRP response while low-grade inflammation shows only minor CRP elevation. The inflammatory response to infection and tissue injury supports host defense, clearance of necrotic tissue, adaptation, and repair, while the purpose of low grade inflammation appears to be restoration of metabolic homeostasis. The factors that trigger the acute inflammatory response and low-grade inflammation differ as well. Acute inflammation is largely triggered by components of an invading pathogen, referred to as pathogen-associated molecular patterns (PAMPs), and by products of damaged cells, damage- (or danger-) associated molecular patterns (DAMPs). The latter are sometimes referred to as alarmins . One molecular mechanism that can trigger low-grade inflammation and CRP induction in response to metabolic stress that has been well-studied is the unfolded protein response . These differences between acute inflammation and low-grade inflammation are so great that two leading researchers in the field have suggested distinct nomenclatures for the latter; both "para-inflammation" and "metaflammation" (metabolically-
51
triggered inflammation) have been proposed to emphasize the distinction between metabolic perturbation and inflammation as it is traditionally viewed, both of which may result in increases in CRP levels.
Figure 17.
52 TREATMENT OF UTI;
Picture 18:Oral medications for UTI
53
Picture 19:Parenteral Management of UTI
54 Picture 20
55 Picture 21
56 Picture 22
57 Picture 23
58 Picture 24
59
MATERIALS AND METHODS
Study center;
Institute of Internal Medicine Madras Medical College and Rajiv Gandhi Government General Hospital. Chennai-03.
Study Design;
Single center Observational Study
Sample size;
100 patients with urinary tract infection attending Internal Medicine OPD or admitted in wards based on inclusion & exclusion criteria. The required sample size was calculated based on the formula 4*
(prevalence of disease)*
(1- prevalence of disease) / Error range.
Collaborating Departments;
Institute of Microbiology, MMC & RGGGH,CH-3.
Institute of Radiology ,MMC & RGGGH,CH-3.
Institute of Biochemistry ,MMC & RGGGH,CH-3.
60 Study Duration;
¾ 1 year
Study plan;
Based on previous studies, the mean value of C-reactive protein in upper urinary tract infection was 116.9 mg/L and lower urinary tract infection was 14.5 mg/L[44]. About 100 patients attending general medicine OPD and admitted in general medicine wards were subjected to detailed history taking, clinical examination and investigations such as CBC, Urine culture & Sensitivity, Serum CRP levels, USG KUB,CT- KUB(whenever necessary).
Inclusion criteria;
Patients with urine samples showing positive urine culture and patients showing symptoms of UTI.
Exclusion criteria;
Patients with inflammatory conditions other than UTI, history of trauma, pregnancy, USG proven renal calculi.
61 Serum CRP Assay Method:
C-reactive protein (CRP) levels in human serum based on the catalytic activity of gold nanoparticles and luminol-H2O2 chemiluminescence. The Chemiluminescence intensity in the presence of CRP and its ligand, O phosphorylethanolamine, was greatly enhanced due to the aggregation of Gold Nano Particles after the addition of 0.5M NaCl.
Statistical Analysis Plan:
Data analysed using statistical package - SPSS Software
Consent
All participants / attenders gave written informed consent.
Ethical Committee Approval
Institutional Ethics Committee of Madras Medical College approved the study.
62
RESULTS
Among 100 patients with UTI, 13% of patients belong to the age group of 20-40 years, 41% between 41-60 years, 42% between 61-80 years and 4% of them was above 80 years. The proportion of subjects in each group among various age range are given in table-1 and figure-25.
Age group Frequency Percent
20-40 years 13 13.0
41-60 years 41 41.0
61-80 years 42 42.0
above 80 years 4 4.0
Total 100 100.0
Table 1:Age distibution of patients with UTI
Picture 25:Age distribution of subjects
13%
41% 42%
4%
0%
5%
10%
15%
20%
25%
30%
35%
40%
45%
20‐40 years 41‐60 years 60‐80 years above 80 years
Age group
63
Among 100 cases ,26 were males and 74 were females.
Table 2: Sex wise distribution of cases
SEX Frequency Percent
Male 26 26.0
Female 74 74.0
Total 100 100.0
Figure 26:Gender Distribution of patients
The most common accompanying illness in patients include DM only comprising of about 38%,plus BPH and Cerebrovascular Accident each occupying 2%.
26%
74%
Gender Distribution
Male Female
COM BPH CVA DM DM,BPH DM,CVA DM,SHT Nil Total
Pat 55% and u
0%
5%
10%
15%
20%
25%
30%
35%
40%
45%
50%
MORBID
H A T
T
tients with upper UT
BPH 4%
DITIES
Table 3: Ac
h a diagno I about 45
CVA 4%
C
64 ccompany
Figure
osis of Lo 5%.
DM DM
38%
COMOR
Frequen 4 4 38 2 2 1 49 100 ying Illnes
e 27.
ower urina
M,BPH DM 2%
RBIDITIE
ncy
ss in UTI
ary tract i
,CVA DM,S
2% 1
ES
Per 4 4 3
2 2
4 10
infection o
SHT N
1%
49
rcent 4.0 4.0 38.0
2.0 2.0 1.0 49.0
00.0
occupy
9%
65
Location of UTI Frequency Percent
lower 55 55.0
Upper 45 45.0
Total 100 100.0 Table 4.
Figure 28.
The most common symptoms in patient with lower urinary tract infection include Dysuria(85%), lower abdominal pain(25%), urgency(16%), frequency(13%).
55%
45%
Location of UTI
lower Upper
66 Figure 29.
%
Dysuria 46 84%
urgency 9 16%
frequency 7 13%
lower abdominal pain 14 25%
Table 4.
84%
16% 13%
25%
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
Dysuria urgency frequency lower abdominal pain
Clinical Features for lower UTI
67
The symptoms in patients with infection involving upper urinary tract include Fever (96%),chills(38%),vomiting (36%),loin pain(18%), Diabetic ketoacidosis (13%).
Figure 30
Fever 43 96%
Loin pain 8 18%
Urgency,Frequency 1 2%
Chills 17 38%
Vomiting 16 36%
Nausea 1 2%
DKA 6 13%
Rigor 4 9%
Table 5.
96%
18%
2%
38% 36%
2%
13% 9%
0%
20%
40%
60%
80%
100%
120%
Fever loin pain frequency Chills Vomiting Nausea Dka Rigor
Clinical Features for Upper UTI
68
The bacterial organisms in UTI was of gram negative bacilli of which E.coli was most common present in about 73%.
URINE CULTURE Frequency Percent
Acinetobacter 1 1.0
E.coli 73 73.0
klebsiella 4 4.0
Normal 16 16.0
Proteus 2 2.0
Pseudomonas 4 4.0
Total 100 100.0
Table 6.
Figure 31.
1%
73%
4%
16%
2%
4%
URINE CULTURE
Acinetobacter E.coli
klebsiella Normal Proteus Pseudomonas
69
Ultrasound abdomen & pelvis was done in all patients with symptoms of urinary tract infection which showed cystitis in 30 out of 55 patients with lower urinary tract infection.Other significant findings include prostatomegaly, pyelonephritis, Hydroureteronephrosis.
USG KUB Frequency Percent Grade 1
prostatomegaly
5 5.0
Grade 2
prostatomegaly
2 2.0
Lt.pyelonephritis 2 2.0
Normal 43 43.0
Cystitis 30 30
Rt.HUN 6 6.0
Rt.pyelonephritis 12 12.0
Total 100 100.0
Table 7.
70 Figure 32.
Non contrast CT-KUB was done in all patients with symptoms of upper urinary tract infection which showed better diagnostic value compared to ultrasound abdomen.
CT KUB(IF DONE) Frequency Percent
B/L Pyelonephritis 4 8.5%
Lt.pyelonephritis 15 31.9%
Lt.pyelonephritis with
HUN 1 2.1%
Normal 2 4.3%
Rt.HUN 1 2.1%
Rt.pyelonephritis 18 38.3%
Rt.pyelonephritis with
HUN 6 12.8%
Total 47 100.0%
Table 8.
5%
2% 2%
43%
6%
12%
30%
USG KUB
Grade 1 prostatomegaly Grade 2 prostatomegaly Lt.pyelonephritis NormalRt.HUN
Rt.pyelonephritis cystitis
71 Figure 33.
The mean value of CRP in subjects with upper UTI(159.20) was significantly higher than the mean value of lower UTI(16.16).
Group Statistics
Location of UTI
N Mean Std.
Deviation
Std.
Error Mean
Z test
CRP
LEVELmgL
lower 55 16.1564 10.40704 1.40329 8.574**
Upper 45 159.2089 49.12149 7.32260
**p<0.001
Table 9.
9%
32%
2%
4%
2%
38%
13%
CT KUB(IF DONE)
B/L Pyelonephritis Lt.pyelonephritis
Lt.pyelonephritis with HUN N
Rt.HUN
Rt.pyelonephritis
Rt.pyelonephritis with HUN
